Cytokines and Sickness Behavior

Dantzer, Robert

doi:10.1007/978-1-4615-0323-1_7

Cited by 40 publications

(42 citation statements)

References 60 publications

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“…In considering possible peripheral actions of chemokines, it is important to note that exposure to pathogens results in complex behavioral and physiological responses, such as fever, disruption of feeding and drinking and reduced social and exploratory behaviors known as 'sickness behavior' [23,24,27,39,72]. This 'sickness behavior' is usually associated with conditioned or learned taste aversion, i.e.…”

Section: Discussionmentioning

confidence: 99%

Perturbation of chemokine networks by gene deletion alters the reinforcing actions of ethanol

Blednov

Bergeson

Walker

et al. 2005

Behavioural Brain Research

132

121

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Microarray analysis of human alcoholic brain and cultured cells exposed to ethanol showed significant changes in expression of genes related to immune or inflammatory responses, including chemokines and chemokine receptors. To test the hypothesis that chemokines exhibit previously undiscovered pleiotropic effects important for the behavioral actions of ethanol, we studied mutant mice with deletion of the Ccr2, Ccr5, Ccl2 or Ccl3 genes. Deletion of Ccr2, Ccl2 (females) or Ccl3 in mice resulted in lower preference for alcohol and consumption of lower amounts of alcohol in a two-bottle choice test as compared with wild-type mice. Ethanol treatment (2.5 g/kg, i.p.) induced stronger conditioned taste aversion in Ccr2, Ccl2 or Ccl3 null mutant mice than in controls. Ccr2 and Ccr5 null mutant mice did not differ from wild-type mice in ethanol-induced loss of righting reflex (LORR), but mice lacking Ccl2 or Ccl3 showed longer LORR than wildtype mice. There were no differences between mutant strains and wild-type mice in severity of ethanol-induced withdrawal. Genetic mapping of chromosome 11 for the Ccl2 and Ccl3 genes (46.5 and 47.6 cM, respectively) revealed that an alcohol-induced LORR QTL region was contained within the introgressed region derived from 129/SvJ, which may cause some behavioral phenotypes observed in the null mice. On the contrary, known QTLs on Chr 9 are outside of 129/ SvJ region in Ccr2 and Ccr5 (71.9 and 72.0 cM, respectively) null mutant mice. These data show that disruption of the chemokine network interferes with motivational effects of alcohol.

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Section: Discussionmentioning

confidence: 99%

Perturbation of chemokine networks by gene deletion alters the reinforcing actions of ethanol

Blednov

Bergeson

Walker

et al. 2005

Behavioural Brain Research

132

121

View full text Add to dashboard Cite

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“…In support of this, QoL impairment in colorectal liver metastasis (CLM) patients has been shown to correlate more closely with extent of immune activation than with liver metastasis volume or the serum level of the tumour marker carcinoembryonic antigen (CEA) (Allen-Mersh et al, 1998). In addition, animal studies suggest that immune activated cytokines induce sickness behaviour (Dantzer et al, 1998) that is similar to QoL impairment in humans (Bauhofer et al, 2001). However, a mechanism by which tumour-related immune activation could result in QoL deterioration has not been identified.…”

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confidence: 99%

Serum tryptophan decrease correlates with immune activation and impaired quality of life in colorectal cancer

et al. 2002

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Cancer-related indoleamine (2,3)-dioxygenase up-regulation by interferon-g might influence quality of life by depleting serum tryptophan. We correlated serum tryptophan levels with immune activation and quality of life in patients with colorectal liver metastases. Venous blood was sampled from patients with primary colorectal cancer and from patients with metachronous colorectal liver metastases who completed quality of life and psychological questionnaires. Serum tryptophan, kynurenine, neopterin, interleukin 2 soluble receptor a (IL-2 sRa), soluble tumour necrosis factor receptor I (sTNF RI), interleukin 6, and C-reactive protein were measured. Liver metastasis volume was estimated by computerised tomography, and survival from blood sampling was noted. Sixty-six patients with colorectal cancer were studied (39 males; median age 66 years) of whom 25 had colorectal liver metastases only (17 males; median age 62 years; median liver metastasis volume 208 ml; median survival 234 days). Reduced serum tryptophan was significantly associated with Rotterdam Symptom Checklist physical symptom (r=70.51, P=0.01) and Sickness Impact Profile (r=70.42, P=0.04) scores, and correlated with increased serum neopterin (r=70.36, P=0.003), IL-2 sRa (r=70.51, P=0.01) and sTNF RI (r=70.45, P=0.02) levels. Stepwise regression analyses suggested that serum tryptophan was an independent predictor of Rotterdam Symptom Checklist physical symptom (regression coefficient 720.78, P=0.01) and Sickness Impact Profile (regression coefficient 7109.09, P=0.04) scores. The results supported a role for interferon-g-mediated serum tryptophan decrease in cancer-induced quality of life deterioration.

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“…2,3 Since atopic allergy itself is an IgE-mediated immune system disorder and depression has been shown to be associated with changes in altered immunity, [5][6][7][8][9] it has been postulated that certain immune mediators, for example cytokines, contribute to the mechanism behind both allergic and depressive symptoms. [10][11][12][13] First-degree relatives of asthmatic children apparently exhibit high rates of depression. 14, 15 Wamboldt et al 16 have provided support for the hypothesis of a shared genetic factor between atopy and behavioral as well as emotional symptoms in a study of juvenile twins, and later between atopy and depression involving an adult twin sample.…”

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confidence: 99%

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

et al. 2003

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Several studies have suggested an association between IgE-mediated atopic allergies and depression. The present study extends our understanding about putative gender differences of this association and provides further epidemiological evidence for our previous finding that the association between atopy and depression may be characteristic for females only. In order to clearly determine the presence of atopic disorders and depression, we used more valid tools than had been employed earlier and we had access to a database (the Northern Finland 1966 Birth Cohort), in which individuals were followed up prospectively until the age of 31 years. The information on allergic symptoms, verified by skin-prick tests and comprising data of 5518 individuals, was used to ascertain the presence of atopy. Depression was assessed with the help of Hopkins' Symptom Checklist-25 and self-reported doctor-diagnosed depression. After adjusting for a father's social class, mother's parity, and place of residence, logistic regression analyses showed that the risk of developing depression increased in parallel with the increasing severity of depression and, when compared with nonatopic subjects, was 3.0 to 4.7-fold up in atopic females and statistically significant. In atopic males, the association between atopy and depression was statistically significant only in the highest depression scores, the odds ratio being 6.3-fold. The results indicate that females suffering from atopic diseases might possess an elevated risk of developing depression already during early adulthood. In males, the association between these two disorders is evident only among the most severe manifestations of depression. Possible background theories, that is, genetic abnormalities in serotonin metabolism, HPA-axis dysfunction, and histamine theory are discussed.

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Cytokines and Sickness Behavior

Cited by 40 publications

References 60 publications

Perturbation of chemokine networks by gene deletion alters the reinforcing actions of ethanol

Perturbation of chemokine networks by gene deletion alters the reinforcing actions of ethanol

Serum tryptophan decrease correlates with immune activation and impaired quality of life in colorectal cancer

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

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